Plasma and dietary magnesium and risk of sudden cardiac death in women1,2,3

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Background: Magnesium has antiarrhythmic properties in cellular and experimental models; however, its relation to sudden cardiac death (SCD) risk is unclear.

Objective: We prospectively examined the association between magnesium, as measured in diet and plasma, and risk of SCD.

Design: The analysis was conducted within the Nurses’ Health Study. The association for magnesium intake was examined prospectively in 88,375 women who were free of disease in 1980. Information on magnesium intake, other nutrients, and lifestyle factors was updated every 2–4 y through questionnaires, and 505 cases of sudden or arrhythmic death were documented over 26 y of follow-up. For plasma magnesium, a nested case-control analysis including 99 SCD cases and 291 controls matched for age, ethnicity, smoking, and presence of cardiovascular disease was performed.

Results: After multivariable adjustment for confounders and potential intermediaries, the relative risk of SCD was significantly lower in women in the highest quartile compared with those in the lowest quartile of dietary (relative risk: 0.63; 95% CI: 0.44, 0.91) and plasma (relative risk: 0.23; 95% CI: 0.09, 0.60) magnesium. The linear inverse relation with SCD was strongest for plasma magnesium (P for trend = 0.003), in which each 0.25-mg/dL (1 SD) increment in plasma magnesium was associated with a 41% (95% CI: 15%, 58%) lower risk of SCD.

Conclusions: In this prospective cohort of women, higher plasma concentrations and dietary magnesium intakes were associated with lower risks of SCD. If the observed association is causal, interventions directed at increasing dietary or plasma magnesium might lower the risk of SCD.

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1

From the Center for Arrhythmia Prevention (SEC and CMA), Division of Preventive Medicine (SEC and CMA), and Cardiovascular Division (CMA), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA; the Department of Nutrition, Harvard School of Public Health, Boston, MA (SEC); the Cardiovascular Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA (ECK and JLJ); and Siemens Healthcare Diagnostics Inc, Newark, DE (MLG).

2

Supported by a research grant from Siemens Healthcare Diagnostics, an Established Investigator Award from the American Heart Association to CMA, and grants CA-87969, HL-34594, HL-03783, and HL-068070 from the National Institutes of Health. JLJ was supported in part by the Balson Cardiac Scholar Fund.

3

Address correspondence to SE Chiuve, Division of Preventive Medicine, 900 Commonwealth Avenue, Boston, MA 02215. E-mail: [email protected].